Intestinal Polyps
Polyps
Adenomatous Polyposis Coli Protein
Adenomatous Polyposis Coli
Genes, APC
Colonic Polyps
Nasal Polyps
Peutz-Jeghers Syndrome
Intestine, Small
Mice, Inbred C57BL
Cyclooxygenase 2
beta Catenin
Anticarcinogenic Agents
Prostaglandin-Endoperoxide Synthases
Mice, Knockout
Gardner's syndrome and steatocystoma multiplex. Two unusual genetically determined conditions occurring in same patient. (1/437)
A 43-year-old man is described who had Gardner's syndrome and steatocystoma multiplex. These two unusual genetically determined conditions were associated because he had inherited the Gardner's syndrome from his father and the steatocystoma multiplex from his mother. (+info)DNA microsatellite instability in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer? (2/437)
AIM: To investigate the distribution of DNA microsatellite instability (MSI) in a series of hyperplastic polyps, serrated adenomas, and mixed polyps of the colorectum. METHODS: DNA was extracted from samples of 73 colorectal polyps comprising tubular adenomas (23), hyperplastic polyps (21), serrated adenomas (17), and mixed polyps (12). The presence of MSI was investigated at six loci: MYCL, D2S123, F13B, BAT-40, BAT-26, and c-myb T22, using polymerase chain reaction based methodology. MSI cases were classified as MSI-Low (MSI-L) and MSI-High (MSI-H), based on the number of affected loci. RESULTS: The frequency of MSI increased in tubular adenomas (13%), hyperplastic polyps (29%), serrated adenomas (53%), and mixed polyps (83%) (Wilcoxon rank sum statistic, p < 0.001). Hyperplastic epithelium was present in nine of 12 mixed polyps and showed MSI in eight of these. MSI was mostly MSI-L. MSI-H occurred in two serrated adenomas and three mixed polyps. Clonal relations were demonstrated between hyperplastic and dysplastic epithelium in four of eight informative mixed polyps. CONCLUSIONS: The findings support the view that hyperplastic polyps may be fundamentally neoplastic rather than hyperplastic. A proportion of hyperplastic polyps may serve as a precursor of a subset (10%) of colorectal cancers showing the MSI-L phenotype, albeit through the intermediate step of serrated dysplasia. This represents a novel and distinct morphogenetic pathway for colorectal cancer. (+info)Controls who experienced hypothetical causal intermediates should not be excluded from case-control studies. (3/437)
It has been suggested that controls with adenomatous polyps of the colon and rectum should be excluded from case-control studies of cigarette smoking and colorectal cancer. A claim has been made that the presence of such controls creates a bias toward the null. The polyps are an intermediate step in a hypothetical causal pathway between the exposure and the disease. Thus, the recommendation logically extends to the exclusion of all controls who experienced hypothetical causal intermediates from all case-control studies. It is shown, in the simple case of an exposure that acts solely through the pathway involving the intermediate, that such exclusions create a bias away from the null. The rationale for recommending the detrimental exclusions appears to stem from a variant of the "trohoc fallacy": the mistaken view of case-control studies as comparisons between diseased and healthy groups and not as comparisons between groups that differ by exposure. (+info)Intestinal polyposis in mice with a dominant stable mutation of the beta-catenin gene. (4/437)
Ectopic expression of certain Wnt genes in mouse mammary tissue is tumorigenic, and mutations that stabilize beta-catenin are found in various human cancers including colorectal cancer. To determine the role of stabilized beta-catenin in intestinal tumorigenesis in mice, we constructed by embryonic stem (ES) cell-mediated homologous recombination, a mutant beta-catenin allele whose exon 3 was sandwiched by loxP sequences. When the germline heterozygotes were crossed with mice expressing Cre recombinase in the intestines, the serines and threonine encoded by exon 3 and to be phosphorylated by glycogen synthase kinase 3beta (GSK3beta) were deleted in the offspring intestines, which caused adenomatous intestinal polyps resembling those in Apc(Delta716) knockout mice. Some nascent microadenomas were also found in the colon. These results present experimental genetic evidence that activation of the Wnt signaling pathway can cause intestinal and colonic tumors. (+info)Immunolocalization of beta catenin in intestinal polyps of Peutz-Jeghers and juvenile polyposis syndromes. (5/437)
AIM: To examine the membranous and nuclear distribution of beta catenin in the epithelial cells of gut polyps from Peutz-Jeghers syndrome and juvenile polyposis in comparison with other types of polyps and tumours. METHODS: Immunohistochemistry for beta catenin and proliferation markers was performed on conventional paraffin sections. Immunohistological staining was carried out on Peutz-Jeghers syndrome polyps from four different families, on juvenile polyposis polyps from two different families, on solitary juvenile polyps, and on hyperplastic polyps. The immunohistochemistry was evaluated qualitatively in relation to defined areas of the polyps. RESULTS: All polyps from the hamartomatous polyposis syndromes (Peutz-Jeghers syndrome and juvenile polyposis) showed nuclear localization of beta catenin in some epithelial cell nuclei. In Peutz-Jeghers syndrome polyps beta catenin positive nuclei were seen at the base of the deep crypt infoldings. In juvenile polyposis polyps and in some solitary juvenile polyps they were found in irregularly distributed cryptal epithelial cells corresponding to the proliferative compartments. Normal mucosa of the gut and hyperplastic polyps of the colon do not show nuclear staining for beta catenin. CONCLUSIONS: The dysregulation of cellular beta catenin distribution is not only a phenomenon of adenoma formation and adenoma progression in the colon--it is at least focally present in polyps of the hamartomatous type and is related to the proliferation zones of these polyps. The nuclear translocation of beta catenin most probably reflects a disturbed beta catenin metabolism. In view of the different functions of beta catenin during development and cell differentiation, the nuclear translocation of beta catenin is likely to be an important factor in enhanced cell proliferation which escapes local control mechanisms. (+info)Anal intraepithelial neoplasia in an inflammatory cloacogenic polyp. (6/437)
A rare case of anal intraepithelial neoplasia arising in an inflammatory cloacogenic polyp is reported. While the occurrence of neoplasia complicating benign anal conditions is recognised, this case re-emphasises the need for careful histological examination of all perianal lesions. (+info)Flexible sigmoidoscopy or colonoscopy as a screening modality for colorectal adenomas in older age groups? Findings in a cohort of the normal population aged 63-72 years. (7/437)
BACKGROUND: Most cases of colorectal cancer originate from adenomas. Removing adenomas has been shown to reduce the incidence of colorectal cancer. The design of cost effective endoscopic screening programmes requires a knowledge of the distribution of adenomas in different age groups. AIM: To investigate the distribution of colorectal adenomas in older age groups in the normal population. METHOD: A total of 356 men and women selected randomly from the population register were offered a colonoscopic screening examination to detect and remove polyps. RESULTS: In all, 241(68%) subjects, mean age 67.4 years (range 62-73), attended. The caecum was intubated in 193 (80%), and in this group 32 (38%) women and 51 (47%) men had adenomas. One hundred and ten (54%) of the adenomas and 11 (39%) of the "high risk adenomas" (adenomas larger than 10 mm in diameter, adenomas containing villous components, and adenomas with severe dysplasia) were found proximal to the sigmoid colon. In 36 (43%) of the subjects with adenomas, the adenomas were only found proximal to the sigmoid colon. Twenty two (11%) subjects had more than two adenomas. Of 203 adenomas discovered, 189 (93%) were less than 10 mm in diameter. CONCLUSION: More than half of the adenomas were localised proximal to the sigmoid colon, and, in nearly half of the adenoma bearing subjects examined, the adenoma was proximal to the descending colon. This indicates that a sigmoidoscopic screening examination in this age group would miss a substantial number of adenomas, but this may be acceptable as the vast majority of proximal adenomas do not progress to clinical cancer within the life expectancy of this age group. (+info)Gastric and duodenal polyps in Smad4 (Dpc4) knockout mice. (8/437)
The SMAD4 (DPC4) gene was initially isolated as a candidate tumor suppressor from the convergent site of homozygous deletions on 18q in a panel of pancreatic carcinoma cell lines. It encodes a common cytoplasmic signaling molecule shared by the transforming growth factor-beta, activin, and bone morphogenic pathways. We recently inactivated its mouse homologue Smad4 and demonstrated its role in the malignant progression of benign adenomas to invasive adenocarcinomas by analyzing mice with Apc and Smad4 compound mutations. Although simple Smad4 homozygotes were embryonically lethal, the heterozygotes were fertile and appeared normal up to the age of 1 year. Upon further investigation, however, they have developed inflammatory polyps in the glandular stomach and duodenum. By PCR genotyping and immunohistochemical staining, the wild-type Smad4 allele has been lost in the polyp epithelial cells, ie., loss of heterozygosity. On the other hand, we have not found any mutations in such genes as K-Ras, H-Ras, N-Ras, p53, or PTEN. Histologically, the polyps are similar to human juvenile polyps showing moderate stromal cell proliferation and infiltrations by eosinophils and plasma cells. In addition, foci of adenocarcinoma with signet ring cells are also found. These results are consistent with a recent report that germ-line SMAD4 mutations are found in a subset of familial juvenile polyposis. (+info)Intestinal polyps are abnormal growths that protrude from the lining of the intestines. They can occur in any part of the digestive tract, including the colon and rectum (colorectal polyps), small intestine, or stomach. These growths vary in size, shape, and number. Most intestinal polyps are benign, meaning they are not cancerous. However, some types of polyps, such as adenomatous polyps, can become cancerous over time if left untreated.
Intestinal polyps can be asymptomatic or cause symptoms like rectal bleeding, abdominal pain, changes in bowel habits, or anemia (in cases where there is chronic, slow bleeding). The exact cause of intestinal polyps is not fully understood, but factors such as age, family history, and certain genetic conditions can increase the risk of developing them. Regular screening exams, like colonoscopies, are essential for early detection and removal of polyps to prevent potential complications, including colorectal cancer.
A polyp is a general term for a small growth that protrudes from a mucous membrane, such as the lining of the nose or the digestive tract. Polyps can vary in size and shape, but they are usually cherry-sized or smaller and have a stalk or a broad base. They are often benign (noncancerous), but some types of polyps, especially those in the colon, can become cancerous over time.
In the digestive tract, polyps can form in the colon, rectum, stomach, or small intestine. Colorectal polyps are the most common type and are usually found during routine colonoscopies. There are several types of colorectal polyps, including:
* Adenomatous polyps (adenomas): These polyps can become cancerous over time and are the most likely to turn into cancer.
* Hyperplastic polyps: These polyps are usually small and benign, but some types may have a higher risk of becoming cancerous.
* Inflammatory polyps: These polyps are caused by chronic inflammation in the digestive tract, such as from inflammatory bowel disease (IBD).
Polyps can also form in other parts of the body, including the nose, sinuses, ears, and uterus. In most cases, polyps are benign and do not cause any symptoms. However, if they become large enough, they may cause problems such as bleeding, obstruction, or discomfort. Treatment typically involves removing the polyp through a surgical procedure.
Adenomatous polyposis coli (APC) protein is a tumor suppressor protein that plays a crucial role in regulating cell growth and division. It is encoded by the APC gene, which is located on chromosome 5. The APC protein helps to prevent excessive cell growth and division by inhibiting the activity of a protein called beta-catenin, which promotes cell growth and division when activated.
In individuals with certain genetic disorders, such as familial adenomatous polyposis (FAP), mutations in the APC gene can lead to the production of a defective APC protein or no APC protein at all. This can result in uncontrolled cell growth and division, leading to the development of numerous benign tumors called polyps in the colon and rectum. Over time, some of these polyps may become cancerous, leading to colorectal cancer if left untreated.
APC protein also has other functions in the body, including regulating cell migration and adhesion, and playing a role in maintaining the stability of the cytoskeleton. Mutations in the APC gene have been linked to other types of cancer besides colorectal cancer, including breast, lung, and ovarian cancers.
Adenomatous Polyposis Coli (APC) is a genetic disorder characterized by the development of numerous adenomatous polyps in the colon and rectum. APC is caused by mutations in the APC gene, which is a tumor suppressor gene that helps regulate cell growth and division. When the APC gene is mutated, it can lead to uncontrolled cell growth and the development of polyps, which can eventually become cancerous.
Individuals with APC typically develop hundreds to thousands of polyps in their colon and rectum, usually beginning in adolescence or early adulthood. If left untreated, APC can lead to colorectal cancer in nearly all affected individuals by the age of 40.
APC is an autosomal dominant disorder, which means that a person has a 50% chance of inheriting the mutated gene from an affected parent. However, some cases of APC may also occur spontaneously due to new mutations in the APC gene. Treatment for APC typically involves surgical removal of the colon and rectum (colectomy) to prevent the development of colorectal cancer. Regular surveillance with colonoscopy is also recommended to monitor for the development of new polyps.
APC (Adenomatous Polyposis Coli) gene is a tumor suppressor gene that provides instructions for making a protein called adenomatous polyposis coli. This protein plays a crucial role in regulating the growth and division of cells in the colon and rectum. Specifically, it helps to maintain the stability of the cell's genetic material (DNA) by controlling the process of beta-catenin degradation.
When the APC gene is mutated or altered, it can lead to an accumulation of beta-catenin in the cell, which can result in uncontrolled cell growth and division. This can ultimately lead to the development of colon polyps, which are benign growths that can become cancerous over time if left untreated.
Mutations in the APC gene are associated with several inherited cancer syndromes, including familial adenomatous polyposis (FAP) and attenuated FAP (AFAP). These conditions are characterized by the development of numerous colon polyps at a young age, which can increase the risk of developing colorectal cancer.
Colonic polyps are abnormal growths that protrude from the inner wall of the colon (large intestine). They can vary in size, shape, and number. Most colonic polyps are benign, meaning they are not cancerous. However, some types of polyps, such as adenomas, have a higher risk of becoming cancerous over time if left untreated.
Colonic polyps often do not cause any symptoms, especially if they are small. Larger polyps may lead to symptoms like rectal bleeding, changes in bowel habits, abdominal pain, or iron deficiency anemia. The exact cause of colonic polyps is not known, but factors such as age, family history, and certain medical conditions (like inflammatory bowel disease) can increase the risk of developing them.
Regular screening exams, such as colonoscopies, are recommended for individuals over the age of 50 to detect and remove polyps before they become cancerous. If you have a family history of colonic polyps or colorectal cancer, your doctor may recommend earlier or more frequent screenings.
Intestinal neoplasms refer to abnormal growths in the tissues of the intestines, which can be benign or malignant. These growths are called neoplasms and they result from uncontrolled cell division. In the case of intestinal neoplasms, these growths occur in the small intestine, large intestine (colon), rectum, or appendix.
Benign intestinal neoplasms are not cancerous and often do not invade surrounding tissues or spread to other parts of the body. However, they can still cause problems if they grow large enough to obstruct the intestines or cause bleeding. Common types of benign intestinal neoplasms include polyps, leiomyomas, and lipomas.
Malignant intestinal neoplasms, on the other hand, are cancerous and can invade surrounding tissues and spread to other parts of the body. The most common type of malignant intestinal neoplasm is adenocarcinoma, which arises from the glandular cells lining the inside of the intestines. Other types of malignant intestinal neoplasms include lymphomas, sarcomas, and carcinoid tumors.
Symptoms of intestinal neoplasms can vary depending on their size, location, and type. Common symptoms include abdominal pain, bloating, changes in bowel habits, rectal bleeding, weight loss, and fatigue. If you experience any of these symptoms, it is important to seek medical attention promptly.
Nasal polyps are benign (noncancerous) growths that originate from the lining of your nasal passages or sinuses. They most often occur in the area where the sinuses open into the nasal cavity. Small nasal polyps may not cause any problems. But if they grow large enough, they can block your nasal passages and lead to breathing issues, frequent infections and loss of smell.
Nasal polyps are associated with chronic inflammation due to conditions such as asthma, allergic rhinitis or chronic sinusitis. Treatment typically includes medication to reduce the size of the polyps or surgery to remove them. Even after successful treatment, nasal polyps often return.
Peutz-Jeghers Syndrome (PJS) is a rare genetic disorder characterized by the development of benign tumors called hamartomas in the gastrointestinal tract and pigmented macules on the skin and mucous membranes. The syndrome is caused by mutations in the STK11/LKB1 gene, which is involved in regulating cell growth and division.
Individuals with PJS have an increased risk of developing various types of cancer, including gastrointestinal tract cancers, breast cancer, ovarian cancer, lung cancer, and cervical cancer. The diagnosis of PJS is typically made based on the presence of characteristic clinical features, such as multiple pigmented macules on the skin and mucous membranes, and a history of benign gastrointestinal tumors or family history of PJS.
Management of PJS involves regular surveillance for gastrointestinal tumors and cancer screening, as well as genetic counseling and testing for family members who may be at risk. Treatment options depend on the location and size of the tumors and may include endoscopic removal or surgery.
An adenoma is a benign (noncancerous) tumor that develops from glandular epithelial cells. These types of cells are responsible for producing and releasing fluids, such as hormones or digestive enzymes, into the surrounding tissues. Adenomas can occur in various organs and glands throughout the body, including the thyroid, pituitary, adrenal, and digestive systems.
Depending on their location, adenomas may cause different symptoms or remain asymptomatic. Some common examples of adenomas include:
1. Colorectal adenoma (also known as a polyp): These growths occur in the lining of the colon or rectum and can develop into colorectal cancer if left untreated. Regular screenings, such as colonoscopies, are essential for early detection and removal of these polyps.
2. Thyroid adenoma: This type of adenoma affects the thyroid gland and may result in an overproduction or underproduction of hormones, leading to conditions like hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid).
3. Pituitary adenoma: These growths occur in the pituitary gland, which is located at the base of the brain and controls various hormonal functions. Depending on their size and location, pituitary adenomas can cause vision problems, headaches, or hormonal imbalances that affect growth, reproduction, and metabolism.
4. Liver adenoma: These rare benign tumors develop in the liver and may not cause any symptoms unless they become large enough to press on surrounding organs or structures. In some cases, liver adenomas can rupture and cause internal bleeding.
5. Adrenal adenoma: These growths occur in the adrenal glands, which are located above the kidneys and produce hormones that regulate stress responses, metabolism, and blood pressure. Most adrenal adenomas are nonfunctioning, meaning they do not secrete excess hormones. However, functioning adrenal adenomas can lead to conditions like Cushing's syndrome or Conn's syndrome, depending on the type of hormone being overproduced.
It is essential to monitor and manage benign tumors like adenomas to prevent potential complications, such as rupture, bleeding, or hormonal imbalances. Treatment options may include surveillance with imaging studies, medication to manage hormonal issues, or surgical removal of the tumor in certain cases.
Adenomatous polyps, also known as adenomas, are benign (noncancerous) growths that develop in the lining of the glandular tissue of certain organs, most commonly occurring in the colon and rectum. These polyps are composed of abnormal glandular cells that can grow excessively and form a mass.
Adenomatous polyps can vary in size, ranging from a few millimeters to several centimeters in diameter. They may be flat or have a stalk (pedunculated). While adenomas are generally benign, they can potentially undergo malignant transformation and develop into colorectal cancer over time if left untreated. The risk of malignancy increases with the size of the polyp and the presence of certain histological features, such as dysplasia (abnormal cell growth).
Regular screening for adenomatous polyps is essential to detect and remove them early, reducing the risk of colorectal cancer. Screening methods include colonoscopy, sigmoidoscopy, and stool-based tests.
The small intestine is the portion of the gastrointestinal tract that extends from the pylorus of the stomach to the beginning of the large intestine (cecum). It plays a crucial role in the digestion and absorption of nutrients from food. The small intestine is divided into three parts: the duodenum, jejunum, and ileum.
1. Duodenum: This is the shortest and widest part of the small intestine, approximately 10 inches long. It receives chyme (partially digested food) from the stomach and begins the process of further digestion with the help of various enzymes and bile from the liver and pancreas.
2. Jejunum: The jejunum is the middle section, which measures about 8 feet in length. It has a large surface area due to the presence of circular folds (plicae circulares), finger-like projections called villi, and microvilli on the surface of the absorptive cells (enterocytes). These structures increase the intestinal surface area for efficient absorption of nutrients, electrolytes, and water.
3. Ileum: The ileum is the longest and final section of the small intestine, spanning about 12 feet. It continues the absorption process, mainly of vitamin B12, bile salts, and any remaining nutrients. At the end of the ileum, there is a valve called the ileocecal valve that prevents backflow of contents from the large intestine into the small intestine.
The primary function of the small intestine is to absorb the majority of nutrients, electrolytes, and water from ingested food. The mucosal lining of the small intestine contains numerous goblet cells that secrete mucus, which protects the epithelial surface and facilitates the movement of chyme through peristalsis. Additionally, the small intestine hosts a diverse community of microbiota, which contributes to various physiological functions, including digestion, immunity, and protection against pathogens.
C57BL/6 (C57 Black 6) is an inbred strain of laboratory mouse that is widely used in biomedical research. The term "inbred" refers to a strain of animals where matings have been carried out between siblings or other closely related individuals for many generations, resulting in a population that is highly homozygous at most genetic loci.
The C57BL/6 strain was established in 1920 by crossing a female mouse from the dilute brown (DBA) strain with a male mouse from the black strain. The resulting offspring were then interbred for many generations to create the inbred C57BL/6 strain.
C57BL/6 mice are known for their robust health, longevity, and ease of handling, making them a popular choice for researchers. They have been used in a wide range of biomedical research areas, including studies of cancer, immunology, neuroscience, cardiovascular disease, and metabolism.
One of the most notable features of the C57BL/6 strain is its sensitivity to certain genetic modifications, such as the introduction of mutations that lead to obesity or impaired glucose tolerance. This has made it a valuable tool for studying the genetic basis of complex diseases and traits.
Overall, the C57BL/6 inbred mouse strain is an important model organism in biomedical research, providing a valuable resource for understanding the genetic and molecular mechanisms underlying human health and disease.
Cyclooxygenase-2 (COX-2) is an enzyme involved in the synthesis of prostaglandins, which are hormone-like substances that play a role in inflammation, pain, and fever. COX-2 is primarily expressed in response to stimuli such as cytokines and growth factors, and its expression is associated with the development of inflammation.
COX-2 inhibitors are a class of nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively block the activity of COX-2, reducing the production of prostaglandins and providing analgesic, anti-inflammatory, and antipyretic effects. These medications are often used to treat pain and inflammation associated with conditions such as arthritis, menstrual cramps, and headaches.
It's important to note that while COX-2 inhibitors can be effective in managing pain and inflammation, they may also increase the risk of cardiovascular events such as heart attack and stroke, particularly when used at high doses or for extended periods. Therefore, it's essential to use these medications under the guidance of a healthcare provider and to follow their instructions carefully.
Beta-catenin is a protein that plays a crucial role in gene transcription and cell-cell adhesion. It is a key component of the Wnt signaling pathway, which regulates various processes such as cell proliferation, differentiation, and migration during embryonic development and tissue homeostasis in adults.
In the absence of Wnt signals, beta-catenin forms a complex with other proteins, including adenomatous polyposis coli (APC) and axin, which targets it for degradation by the proteasome. When Wnt ligands bind to their receptors, this complex is disrupted, allowing beta-catenin to accumulate in the cytoplasm and translocate to the nucleus. In the nucleus, beta-catenin interacts with T cell factor/lymphoid enhancer-binding factor (TCF/LEF) transcription factors to activate the transcription of target genes involved in cell fate determination, survival, and proliferation.
Mutations in the genes encoding components of the Wnt signaling pathway, including beta-catenin, have been implicated in various human diseases, such as cancer, developmental disorders, and degenerative conditions.
Anticarcinogenic agents are substances that prevent, inhibit or reduce the development of cancer. They can be natural or synthetic compounds that interfere with the process of carcinogenesis at various stages, such as initiation, promotion, and progression. Anticarcinogenic agents may work by preventing DNA damage, promoting DNA repair, reducing inflammation, inhibiting cell proliferation, inducing apoptosis (programmed cell death), or modulating immune responses.
Examples of anticarcinogenic agents include chemopreventive agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and retinoids; phytochemicals found in fruits, vegetables, and other plant-based foods; and medications used to treat cancer, such as chemotherapy, radiation therapy, and targeted therapies.
It is important to note that while some anticarcinogenic agents have been shown to be effective in preventing or reducing the risk of certain types of cancer, they may also have potential side effects and risks. Therefore, it is essential to consult with a healthcare professional before using any anticarcinogenic agent for cancer prevention or treatment purposes.
Colonic neoplasms refer to abnormal growths in the large intestine, also known as the colon. These growths can be benign (non-cancerous) or malignant (cancerous). The two most common types of colonic neoplasms are adenomas and carcinomas.
Adenomas are benign tumors that can develop into cancer over time if left untreated. They are often found during routine colonoscopies and can be removed during the procedure.
Carcinomas, on the other hand, are malignant tumors that invade surrounding tissues and can spread to other parts of the body. Colorectal cancer is the third leading cause of cancer-related deaths in the United States, and colonic neoplasms are a significant risk factor for developing this type of cancer.
Regular screenings for colonic neoplasms are recommended for individuals over the age of 50 or those with a family history of colorectal cancer or other risk factors. Early detection and removal of colonic neoplasms can significantly reduce the risk of developing colorectal cancer.
Prostaglandin-Endoperoxide Synthases (PTGS), also known as Cyclooxygenases (COX), are a group of enzymes that catalyze the conversion of arachidonic acid into prostaglandin G2 and H2, which are further metabolized to produce various prostaglandins and thromboxanes. These lipid mediators play crucial roles in several physiological processes such as inflammation, pain, fever, and blood clotting. There are two major isoforms of PTGS: PTGS-1 (COX-1) and PTGS-2 (COX-2). While COX-1 is constitutively expressed in most tissues and involved in homeostatic functions, COX-2 is usually induced during inflammation and tissue injury. Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their therapeutic effects by inhibiting these enzymes, thereby reducing the production of prostaglandins and thromboxanes.
A "knockout" mouse is a genetically engineered mouse in which one or more genes have been deleted or "knocked out" using molecular biology techniques. This allows researchers to study the function of specific genes and their role in various biological processes, as well as potential associations with human diseases. The mice are generated by introducing targeted DNA modifications into embryonic stem cells, which are then used to create a live animal. Knockout mice have been widely used in biomedical research to investigate gene function, disease mechanisms, and potential therapeutic targets.